Our study has several limitations including 1) the observational nature of the study, 2) potential for linkage disequilibrium, 3) lack of assessment of dynamic changes in serum lipoproteins, PCSK9, and endothelial dysfunction markers, 4) potential for unadjusted confounders, and 5) fundamental biological differences with regard to lipoprotein metabolism such as the lack of cholesteryl ester transfer protein (CETP) among mice. This evidence concerns the gene PCSK9 and endothelial dysfunction.